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Inflammation

Inflammation
the injured tissues. A cascade of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells which are present at the site of inflammation and is characterised by simultaneous destruction and healing of the tissue from the inflammatory process.

Causes
An abscess on the skin, showing the redness and swelling characteristic of inflammation. Black rings of necrotic tissue surround central areas of pus Inflammation (Latin, inflamatio, to set on fire) is the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants.[1] It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. Inflammation is not a synonym for infection. Even in cases where inflammation is caused by infection, the two are not synonymous: infection is caused by an exogenous pathogen, while inflammation is the response of the organism to the pathogen. In the absence of inflammation, wounds and infections would never heal and progressive destruction of the tissue would compromise the survival of the organism. However, an inflammation that runs unchecked can also lead to a host of diseases, such as hay fever, atherosclerosis, and rheumatoid arthritis. It is for that reason that inflammation is normally closely regulated by the body. Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes from the blood into • • • • • • • • • Burns Chemical irritants Frostbite Toxins Infection by pathogens Physical injury, blunt or penetrating Immune reactions due to hypersensitivity Ionizing radiation Foreign bodies, including splinters and dirt

Types
Comparison between acute and chronic inflammation: Acute Causative agent
Pathogens, injured tissues

Chronic
Persistent acute inflammation due to non-degradable pathogens, persistent foreign bodies, or autoimmune reactions

Major cells involved

Neutrophils, mononuclear cells (monocytes,

Mononuclear cells (monocytes, macrophages, plasma cells), fibroblasts

macrophages) lymphocytes,

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Primary mediators
Vasoactive amines, eicosanoids IFN-γ and other cytokines, growth factors, reactive oxygen species, hydrolytic enzymes

Inflammation

Onset Duration

Immediate Few days

Delayed Up to many months, or years

Outcomes

Resolution, abscess forminflammation

Tissue destruction,

ation, chronic fibrosis

Infected ingrown toenail showing the characteristic redness and swelling associated with acute inflammation Redness and heat are due to increased blood flow at body core temperature to the inflamed site; swelling is caused by accumulation of fluid; pain is due to release of chemicals that stimulate nerve endings. Loss of function has multiple causes.[5] These five signs appear when acute inflammation occurs on the body’s surface, whereas acute inflammation of internal organs may not result in the full set. Pain only happens where the appropriate sensory nerve endings exist in the inflamed area — e.g., acute inflammation of the lung (pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings.[5]

Clinical signs
The classic signs and symptoms of acute inflammation: English Redness Swelling Heat Pain Loss of function Rubor* Tumor/Turgor* Calor* Dolor* Functio laesa** Latin

All the above signs may be observed in specific instances, but no single sign must, as a matter of course, be present. inflammation.
[2] [2]

These are the original, so called, "cardinal signs" of * Functio laesa is a bit of an apocryphal notion, as it is not really unique to inflammation and is a characteristic of many disease states.
[3]**

Process of acute inflammation
The process of acute inflammation is initiated by cells already present in all tissues, mainly resident macrophages such as dendritic cells, histiocytes, Kuppfer cells and mastocytes. Once activated by infection, burn, or other injuries, the cells undergo activation and release inflammatory mediators responsible for the signs of inflammation. Vasodilation and its resulting increased blood flow causes the redness (rubor) and increased heat (calor). Increased permeability of the blood vessels results in an exudation (leakage) of plasma proteins and fluid into the tissue (Edema), manifesting as swelling (tumor). Some of the released mediators such as bradykinin increase the sensitivity to pain (hyperalgesia, dolor). The mediator molecules also alter the blood vessels to permit the migration of leukocytes, mainly neutrophils, outside of the

Acute inflammation is a short-term process, usually appearing in a few minutes or hours and ceasing once the injurious stimulus has been removed.[4]. It is characterized by five cardinal signs:[5] • rubor (redness), • calor (increased heat), • tumor (swelling), • dolor (pain), and • functio laesa (loss of function). The first four (classical signs) were described by Celsus (ca 30 BC–38 AD), while loss of function was added later by Virchow in 1870.[5][4]

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blood vessels (extravasation) into the tissue. The neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury. [4] The loss of function (functio laesa) is probably the result of a neurological reflex in response to pain. In addition to cell-derived mediators, several acellular biochemical cascade systems consisting of preformed plasma proteins act in parallel to initiate and propagate the inflammatory response. These include the complement system activated by bacteria, and the coagulation and fibrinolysis systems activated by necrosis, e.g. a burn or a trauma.
[4]

Inflammation
periphery of the vessels moves cells in the blood into the middle of the vessel.

Plasma cascade systems
• The complement system, when activated, results in the increased removal of pathogens via opsonisation and phagocytosis. • The kinin system generates proteins capable of sustaining vasodilation and other physical inflammatory effects. • The coagulation system or clotting cascade which forms a protective protein mesh over sites of injury. • The fibrinolysis system, which acts in opposition to the coagulation system, to counterbalance clotting and generate several other inflammatory mediators.

The acute inflammatory response requires constant stimulation to be sustained. Inflammatory mediators have short half lives and are quickly degraded in the tissue. Hence, inflammation ceases once the stimulus has been removed.[4]

Plasma derived mediators
* non-exhaustive list

Exudative component
The exudative component involves the movement of plasma fluid, containing important proteins such as fibrin and immunoglobulins (antibodies), into inflamed tissue. This movement is achieved via the chemically induced dilation and increased permeability of blood vessels, which results in a net loss of blood plasma. The increased collection of fluid into the tissue causes it to swell (edema).

Cellular component
The cellular component involves leukocytes, which normally reside in blood and must move into the inflamed tissue via extravasation to aid in inflammation. Some act as phagocytes, ingesting bacteria, viruses, and cellular debris. Others release enzymatic granules which damage pathogenic invaders. Leukocytes also release inflammatory mediators which develop and maintain the inflammatory response. Generally speaking, acute inflammation is mediated by granulocytes, while chronic inflammation is mediated by mononuclear cells such as monocytes and lymphocytes.

Vascular changes
Acute inflammation is characterised by marked vascular changes, including vasodilation, increased permeability, and the slowing of blood flow, which are induced by the actions of various inflammatory mediators. Vasodilation occurs first at the arteriole level, progressing to the capillary level, and brings about a net increase in the amount of blood present, causing the redness and heat of inflammation. Increased permeability of the vessels results in the movement of plasma into the tissues, with resultant stasis due to the increase in the concentration of the cells within blood - a condition characterised by enlarged vessels packed with cells. Stasis allows leukocytes to marginate along the endothelium, a process critical to their recruitment into the tissues. Normal flowing blood prevents this, as the shearing force along the

Leukocyte extravasation
Various leukocytes are critically involved in the initiation and maintenance of inflammation. These cells must be able to get to the site of injury from their usual location in the blood, therefore mechanisms exist to recruit and direct leukocytes to the appropriate place. The process of leukocyte movement from the blood to the tissues through the blood vessels is known as extravasation, and can be divided up into a number of broad steps: 1. Recruitment of leukocytes is receptormediated. The products of inflammation, such as histamine, promote the immediate expression of P-selectin on endothelial cell

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Name Produced by Description

Inflammation

Bradykinin Kinin system C3

A vasoactive protein which is able to induce vasodilation, increase vascular permeability, cause smooth muscle contraction, and induce pain.

Complement Cleaves to produce C3a and C3b. C3a stimulates histamine resystem lease by mast cells, thereby producing vasodilation. C3b is able to bind to bacterial cell walls and act as an opsonin, which marks the invader as a target for phagocytosis. Complement Stimulates histamine release by mast cells, thereby producing vassystem odilation. It is also able to act as a chemoattractant to direct cells via chemotaxis to the site of inflammation. A protein which circulates inactively, until activated by collagen, platelets, or exposed basement membranes via conformational change. When activated, it in turn is able to activate three plasma systems involved in inflammation: the kinin system, fibrinolysis system, and coagulation system.

C5a

Factor XII Liver (Hageman Factor)

Membrane Complement A complex of the complement proteins C5b, C6, C7, C8, and mulsystem tiple units of C9. The combination and activation of this range of attack complement proteins forms the membrane attack complex, which complex is able to insert into bacterial cell walls and causes cell lysis with ensuing death. Plasmin Thrombin Fibrinolysis Able to break down fibrin clots, cleave complement protein C3, system and activate Factor XII. Coagulation Cleaves the soluble plasma protein fibrinogen to produce insoluble system fibrin, which aggregates to form a blood clot. Thrombin can also bind to cells via the PAR1 receptor to trigger several other inflammatory responses, such as production of chemokines and nitric oxide. 3. Leukocytes reaching the tissue interstitium bind to extracellular matrix proteins via expressed integrins and CD44 to prevent their loss from the site. Chemoattractants cause the leukocytes to move along a chemotactic gradient towards the source of inflammation.

surfaces. This receptor binds weakly to carbohydrate ligands on leukocyte surfaces and causes them to "roll" along the endothelial surface as bonds are made and broken. Cytokines from injured cells induce the expression of E-selectin on endothelial cells, which functions similarly to P-selectin. Cytokines also induce the expression of integrin ligands on endothelial cells, which further slow leukocytes down. These weakly bound leukocytes are free to detach if not activated by chemokines produced in injured tissue. Activation increases the affinity of bound integrin receptors for ligands on the endothelial cell surface, firmly binding the leukocytes to the endothelium. 2. Chemokine gradients stimulate the adhered leukocytes to move between endothelial cells and pass the basement membrane into the tissues.

Cell derived mediators
* non-exhaustive list

Morphologic patterns
Specific patterns of acute and chronic inflammation are seen during particular situations that arise in the body, such as when inflammation occurs on an epithelial surface, or pyogenic bacteria are involved. • characterised by the formation of granulomas, they are the result of a limited but diverse number of diseases, which include among others tuberculosis, leprosy, and syphilis.

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Name Lysosome granules Type Enzymes Source Description

Inflammation

Granulocytes These cells contain a large variety of enzymes which perform a number of functions. Granules can be classified as either specific or azurophilic depending upon the contents, and are able to break down a number of substances, some of which may be plasma-derived proteins which allow these enzymes to act as inflammatory mediators. Stored in preformed granules, histamine is released in response to a number of stimuli. It causes arteriole dilation and increased venous permeability. Antiviral, immunoregulatory, and anti-tumour properties. This interferon was originally called macrophage-activating factor, and is especially important in the maintenance of chronic inflammation.

Histamine

Vasoactive Mast cells, amine basophils, platelets Cytokine T-cells, NK cells

IFN-γ

IL-8

Chemokine Primarily Activation and chemoattraction of neutrophils, macrophages with a weak effect on monocytes and eosinophils. Eicosanoid Leukocytes Able to mediate leukocyte adhesion and activation, allowing them to bind to the endothelium and migrate across it. In neutrophils, it is also a potent chemoattractant, and is able to induce the formation of reactive oxygen species and the release of lysosome enzymes by these cells. Potent vasodilator, relaxes smooth muscle, reduces platelet aggregation, aids in leukocyte recruitment, direct antimicrobial activity in high concentrations. A group of lipids which can cause vasodilation, fever, and pain.

Leukotriene B4

Nitric oxide

Soluble gas

Macrophages, endothelial cells, some neurons

Prostaglandins Eicosanoid Mast cells TNF-α and IL-1 Cytokines

Primarily Both affect a wide variety of cells to induce macrophages many similar inflammatory reactions: fever, production of cytokines, endothelial gene regulation, chemotaxis, leukocyte adherence, activation of fibroblasts. Responsible for the systemic effects of inflammation, such as loss of appetite and increased heart rate. cells, and fluid. Infection by pyogenic bacteria such as staphylococci is characteristic of this kind of inflammation. Large, localised collections of pus enclosed by surrounding tissues are called abscesses. • Characterised by the copious effusion of non-viscous serous fluid, commonly produced by mesothelial cells of serous membranes, but may be derived from blood plasma. Skin blisters exemplify this pattern of inflammation.

• Inflammation resulting in a large increase in vascular permeability allows fibrin to pass through the blood vessels. If an appropriate procoagulative stimulus is present, such as cancer cells,[4] a fibrinous exudate is deposited. This is commonly seen in serous cavities, where the conversion of fibrinous exudate into a scar can occur between serous membranes, limiting their function. • Inflammation resulting in large amount of pus, which consists of neutrophils, dead

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From Wikipedia, the free encyclopedia
• • • • • • • • • • •

Inflammation
Autoimmune diseases Chronic inflammation Chronic prostatitis Glomerulonephritis Hypersensitivities Inflammatory bowel diseases Pelvic inflammatory disease Reperfusion injury Rheumatoid arthritis Transplant rejection Vasculitis

Allergies
An allergic reaction, formally known as type 1 hypersensitivity, is the result of an inappropriate immune response triggering inflammation. A common example is hay fever, which is caused by a hypersensitive response by skin mast cells to allergens. Pre-sensitised mast cells respond by degranulating, releasing vasoactive chemicals such as histamine. These chemicals propagate an excessive inflammatory response characterised by blood vessel dilation, production of pro-inflammatory molecules, cytokine release, and recruitment of leukocytes.[4] Severe inflammatory response may mature into a systemic response known as anaphylaxis. Other hypersensitivity reactions (type 2 and type 3) are mediated by antibody reactions and induce inflammation by attracting leukocytes which damage surrounding tissue.[4]

Neutrophils migrate from blood vessels to the inflamed tissue via chemotaxis, where they remove pathogens through phagocytosis and degranulation • Inflammation occurring near an epithelium can result in the necrotic loss of tissue from the surface, exposing lower layers. The subsequent excavation in the epithelium is known as an ulcer.

Inflammatory disorders
Abnormalities associated with inflammation comprise a large, unrelated group of disorders which underlie a variety of human diseases. The immune system is often involved with inflammatory disorders, demonstrated in both allergic reactions and some myopathies, with many immune system disorders resulting in abnormal inflammation. Non-immune diseases with a etiological origins in inflammatory processes are thought to include cancer, atherosclerosis, and ischaemic heart disease.[4] A large variety of proteins are involved in inflammation, and any one of them is open to a genetic mutation which impairs or otherwise dysregulates the normal function and expression of that protein. Examples of disorders associated with inflammation include: • Asthma

Myopathies
Inflammatory myopathies are caused by the immune system inappropriately attacking components of muscle, leading to signs of muscle inflammation. They may occur in conjunction with other immune disorders, such as systemic sclerosis, and include dermatomyositis, polymyositis, and inclusion body myositis.[4]

Leukocyte defects
Due to the central role of leukocytes in the development and propagation of inflammation, defects in leukocyte function often result in a decreased capacity for inflammatory defense with subsequent vulnerability to infection.[4] Dysfunctional leukocytes may be unable to correctly bind to blood vessels due to surface receptor mutations, digest bacteria (Chediak-Higashi syndrome), or produce microbicides (chronic granulomatous

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disease). Additionally, diseases affecting the bone marrow may result in abnormal or few leukocytes.

Inflammation
termination sequence. Neutrophil recruitment thus ceases and programmed death by apoptosis is engaged. These events coincide with the biosynthesis, from omega-3 polyunsaturated fatty acids, of resolvins and protectins, which critically shorten the period of neutrophil infiltration by initiating apoptosis. Consequently, apoptotic neutrophils undergo phagocytosis by macrophages, leading to neutrophil clearance and release of anti-inflammatory and reparative cytokines such as transforming growth factor-Β1. The anti-inflammatory program ends with the departure of macrophages through the lymphatics.[8] —Charles Serhan

Pharmacological
Certain drugs or chemical compounds are known to affect inflammation. Vitamin A deficiency causes an increase in inflammatory responses,[6] and anti-inflammatory drugs work specifically by inhibiting normal inflammatory components.

Cancer
Inflammation orchestrates the microenvironment around tumours, contributing to proliferation, survival and migration. Cancer cells use selectins, chemokines and their receptors for invasion, migration and metastasis.[7] On the other hand, many cells of the immune system contribute to cancer immunology, suppressing cancer.

Systemic effects
An organism can escape the confines of the immediate tissue via the circulatory system or lymphatic system, where it may spread to other parts of the body. If an organism is not contained by the actions of acute inflammation it may gain access to the lymphatic system via nearby lymph vessels. An infection of the lymph vessels is known as lymphangitis, and infection of a lymph node is known as lymphadenitis. A pathogen can gain access to the bloodstream through lymphatic drainage into the circulatory system. When inflammation overwhelms the host, systemic inflammatory response syndrome is diagnosed. When it is due to infection, the term sepsis is applied, with bacteremia being applied specifically for bacterial sepsis and viremia specifically to viral sepsis. Vasodilation and organ dysfunction are serious problems associated with widespread infection that may lead to septic shock and death.

Termination
The inflammatory response must be actively terminated when no longer needed to prevent unnecessary "bystander" damage to tissues.[4] Failure to do so results in chronic inflammation, cellular destruction, and attempts to heal the inflamed tissue. One intrinsic mechanism employed to terminate inflammation is the short half-life of inflammatory mediators in vivo. They have a limited time frame to affect their target before breaking down into non-functional components, therefore constant inflammatory stimulation is needed to propagate their effects. Active mechanisms which serve to terminate inflammation include[4]: • TGF-β from macrophages • Anti-inflammatory lipoxins • Inhibition of pro-inflammatory molecules, such as leukotrienes “ Acute inflammation normally resolves by mechanisms that have remained somewhat elusive. Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins. After entering tissues, granulocytes promote the switch of arachidonic acid–derived prostaglandins and leukotrienes to lipoxins, which initiate the ”

Acute-phase proteins
Inflammation also induces high systemic levels of acute-phase proteins. In acute inflammation, these proteins prove beneficial, however in chronic inflammation they can contribute to amyloidosis.[4] These proteins include C-reactive protein, serum amyloid A, and serum amyloid P, vasopressin, which cause a range of systemic effects including[4]: • Fever

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• • • • • Increased blood pressure Decreased sweating Malaise Loss of appetite Somnolence

Inflammation

Leukocyte numbers
Inflammation often affects the numbers of leukocytes present in the body: • Leukocytosis is often seen during inflammation induced by infection, where it results in a large increase in the amount of leukocytes in the blood, especially immature cells. Leukocyte numbers usually increase to between 15 000 and 20 000 cells per ml, but extreme cases can see it approach 100 000 cells per ml.[4] Bacterial infection usually results in an increase of neutrophils, creating neutrophilia, whereas diseases such as asthma, hay fever, and parasite infestation result in an increase in eosinophils, creating eosinophilia.[4] • Leukopenia can be induced by certain infections and diseases, including viral infection, Rickettsia infection, some protozoa, tuberculosis, and some cancers.[4]

Scars present on the skin, evidence of fibrosis and healing of a wound that is causing it. Here are the possible outcomes to inflammation:[4] 1. The complete restoration of the inflamed tissue back to a normal status. Inflammatory measures such as vasodilation, chemical production, and leukocyte infiltration cease, and damaged parenchymal cells regenerate. In situations where limited or short lived inflammation has occurred this is usually the outcome. 2. Large amounts of tissue destruction, or damage in tissues unable to regenerate, can not be regenerated completely by the body. Fibrous scarring occurs in these areas of damage, forming a scar composed primarily of collagen. The scar will not contain any specialized structures, such as parenchymal cells, hence functional impairment may occur. 3. A cavity is formed containing pus, an opaque liquid containing dead white blood cells and bacteria with general debris from destroyed cells. 4. In acute inflammation, if the injurious agent persists then chronic inflammation will ensue. This process, marked by inflammation lasting many days, months or even years, may lead to the formation of a chronic wound. Chronic inflammation is characterised by the dominating presence of macrophages in the injured tissue. These cells are powerful defensive agents of the body, but the toxins they

Systemic inflammation and obesity
With the discovery of interleukins (IL), the concept of systemic inflammation developed. Although the processes involved are identical to tissue inflammation, systemic inflammation is not confined to a particular tissue but involves the endothelium and other organ systems. High levels of several inflammation-related markers such as IL-6, IL-8, and TNF-α are associated with obesity.[9][10] During clinical studies, inflammatory-related molecule levels were reduced and increased levels of anti-inflammatory molecules were seen within four weeks after patients began a very low calorie diet.[11] The association of systemic inflammation with insulin resistance and atherosclerosis is the subject of intense research.[12]

Outcomes
The outcome in a particular circumstance will be determined by the tissue in which the injury has occurred and the injurious agent

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release (including reactive oxygen species) are injurious to the organism’s own tissues as well as invading agents. Consequently, chronic inflammation is almost always accompanied by tissue destruction.

Inflammation

Examples
Inflammation is usually indicated by adding the suffix "-itis", as shown below. However, some conditions such as asthma and pneumonia do not follow this convention. More examples are available at list of types of inflammation.

Acute Acute appendicitis dermatitis Acute infective meningitis

Acute tonsillitis

See also
• • • • • • Anaphylatoxin Anti-inflammatories Healing Interleukin Lipoxin Substance P

References
[1] Ferrero-Miliani L, Nielsen OH, Andersen PS, Girardin SE (February 2007). "Chronic inflammation: importance of NOD2 and NALP3 in interleukin-1beta generation". Clin. Exp. Immunol. 147 (2): 227–35. doi:10.1111/ j.1365-2249.2006.03261.x. PMID 17223962. [2] ^ Stedman’s Medical Dictionary, Twenty-fifth Edition, Williams & Wilkins, 1990. [3] Disturbance of function (functio laesa): the legendary fifth cardinal sign of inflammation, added by Galen to the four cardinal signs of Celsus. Bull N Y Acad Med. 1971 March; 47(3): 303–322 [4] ^ Cotran; Kumar, Collins (1998). Robbins Pathologic Basis of Disease.

Philadelphia: W.B Saunders Company. ISBN 0-7216-7335-X. [5] ^ Parakrama Chandrasoma, Clive R. Taylor (ca. 2005). "Part A. General Pathology, Section II. The Host Response to Injury, Chapter 3. The Acute Inflammatory Response, sub-section Cardinal Clinical Signs". Concise Pathology (3rd edition (Computer file) ed.). New York, N.Y.: McGraw-Hill. ISBN 0838514995. OCLC 150148447. http://www.accessmedicine.com/ content.aspx?aID=183351. Retrieved on 2008-11-05. [6] Wiedermann U, et al (1996). "Vitamin A deficiency increases inflammatory responses.". Scand J Immunol. 44 (6): 578–84. doi:10.1046/ j.1365-3083.1996.d01-351.x. PMID 8972739. http://www.ncbi.nlm.nih.gov/ entrez/ query.fcgi?db=pubmed&list_uids=8972739&cmd=R [7] Coussens LM, Werb Z (2002). "Inflammation and cancer". Nature 420 (6917): 860–7. doi:10.1038/nature01322. PMID 12490959. [8] Serhan CN, Savill J (2005). "Resolution of inflammation: the beginning programs the end". Nat. Immunol. 6 (12): 1191–7. doi:10.1038/ni1276. PMID 16369558. http://www.nature.com/ni/journal/v6/n12/ abs/ni1276.html. [9] Bastard J et al (2000). "Elevated levels of interleukin 6 are reduced in serum and subcutaneous adipose tissue of obese women after weight loss". J Clin Endocrinol Metab 85 (9): 3338–42. doi:10.1210/jc.85.9.3338. PMID 10999830. http://jcem.endojournals.org/ cgi/content/full/85/9/ 3338?ijkey=c94031a625120a7e59ea52e88137260e9 [10] Mohamed-Ali V et al (2001). "betaAdrenergic regulation of IL-6 release from adipose tissue: in vivo and in vitro studies". J Clin Endocrinol Metab 86 (12): 5864–9. doi:10.1210/jc.86.12.5864. PMID 11739453. http://jcem.endojournals.org/cgi/content/ full/86/12/ 5864?ijkey=838bb038c4e311324ab354c88ea16afe51 [11] Clément K et al (2004). "Weight loss regulates inflammation-related genes in white adipose tissue of obese subjects". Faseb J 18 (14): 1657–69. doi:10.1096/ fj.04-2204com. PMID 15522911.

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http://www.fasebj.org/cgi/content/full/18/ 14/1657. [12] M Stitzinger (2007). "Lipids, inflammation and atherosclerosis" (pdf). The digital repository of Leiden University. https://openaccess.leidenuniv.nl/dspace/ bitstream/1887/9729/11/01.pdf. Retrieved on 2007-11-02.

Inflammation
suppresses NF-kappaB -driven immune responses: regulation of aging via NF-kappaB acetylation? Bioessays. 2008 Oct;30(10):939-42. Rangan G, Wang Y, Harris D. NF-kappaB signalling in chronic kidney disease. Front Biosci. 2009 Jan 1;14:3496-522. Review. PMID: 19273289

Further Reading
Kyriakis JM, Avruch J. Sounding the alarm: protein kinase cascades activated by stress and inflammation. J Biol Chem. 1996 Oct 4;271(40):24313-6. Review. PMID: 8798679 Salminen A, Kauppinen A, Suuronen T, Kaarniranta K. SIRT1 longevity factor

External links
• What You Need to Know About Inflammation at Cleveland Clinic • Anti-Inflammatory Diet - Foods and Inflammation at About.com • MeSH Inflammation

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